Dental Flossing and Its Relationship to Transient Bacteremia

Carroll, Gilbert C.; Sebor, Raymond J.

doi:10.1902/jop.1980.51.12.691

Cited by 90 publications

(83 citation statements)

References 10 publications

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“…This mode of challenge is reasonable because patients with periodontitis are thought to be chronically exposed to nonsymptomatic bacteremias, the level, duration, and microbial diversity of which increase with periodontal disease severity 3 ; dental extraction, periodontal surgery, tooth scaling, and even tooth brushing and flossing can seed oral bacteria into systemic circulation. 10,19 Particularly, bacteremia from a putative pathogen in periodontal disease, Pg, is observed after dental treatment. 20 For this purpose, we intravenously inoculated live Pg into heterozygous ApoE ϩ/Ϫ mice.…”

Section: Discussionmentioning

confidence: 99%

Porphyromonas gingivalis Infection Accelerates the Progression of Atherosclerosis in a Heterozygous Apolipoprotein E–Deficient Murine Model

et al. 2002

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Background-Current epidemiological data suggest that dental infections affecting tooth-supporting tissues (periodontitis) can disseminate into the systemic circulation and thereby contribute to atherosclerosis progression. To test this hypothesis, we investigated the effect of repeated systemic inoculations with Porphyromonas gingivalis (Pg), a putative periodontal pathogen, on the progression of atherosclerosis in heterozygous apolipoprotein E-deficient (ApoE ϩ/Ϫ ) mice. Methods and Results-Ten-week-old, male ApoE ϩ/Ϫ mice fed either a high-fat diet or regular chow were inoculated intravenously with live Pg (10 7 CFU) or vehicle once per week for 10, 14, or 24 consecutive weeks. Histomorphometry of plaque cross-sectional area in the proximal aortas, en face measurement of plaque area over the aortic trees, Pg 16S ribosomal DNA amplification with polymerase chain reaction, ELISA for systemic proinflammatory mediators, and immunolocalization of macrophages in the proximal aorta were performed. Atherosclerotic lesions of the proximal aortas and aortic trees were more advanced in Pg-challenged animals than in vehicle control animals and occurred earlier (at 10 weeks) when no lesions were apparent in control animals. At 24 weeks after inoculation, proximal aortic lesion size quantified by histomorphometry was 9-fold greater in chow-fed mice inoculated with Pg than in noninoculated mice (PϽ0.001) and was 2-fold greater in Pg-inoculated versus noninoculated high-fat diet-fed mice (PϽ0.001); all atherosclerotic lesions were macrophage-rich. Pg ribosomal DNA was found in the aortas, livers, and hearts 24 weeks after inoculation. Conclusions-These

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Section: Discussionmentioning

confidence: 99%

Porphyromonas gingivalis Infection Accelerates the Progression of Atherosclerosis in a Heterozygous Apolipoprotein E–Deficient Murine Model

et al. 2002

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“…It is well established that periodontal organisms such as P. gingivalis have a direct route to the circulatory system by the way of transient bacteremias (the presence of bacteria in the blood) and that these events occur commonly and frequently. [13][14][15][16] Thus, the interactions of P. gingivalis and human coronary artery endothelial cells (HCAEC) may have a significant effect on the progression of atherosclerosis.…”

Section: Introductionmentioning

confidence: 99%

Autophagy: A Highway for Porphyromonas gingivalis in Endothelial Cells

Bélanger

Rodrigues²,

Dunn³

et al. 2006

Autophagy

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“…Type II collagen-specific memory T cells, however, can be found in the joints of rheumatoid arthritis patients (17). Harbored in the dental plaque of humans (12,52), S. sanguis could induce a systemic challenge through ulceration of the epithelial barrier at the gingival sulcus (13,14). The systemic challenge through the gingiva would be expected to exacerbate progression, but not initiate autorecognition in patients harboring type II collagen-specific memory T cells such as in rheumatoid arthritis (17).…”

Section: Discussionmentioning

confidence: 99%

“…Of limited pathogenicity in healthy individuals, S. sanguis can enter the blood periodically through breaches in the dento-gingival junction (13) or the oral mucosae (14). S. sanguis strain 133-79 also expresses a collagen-like epitope (accession A44428) within the platelet aggregation-associated protein (PAAP) 3 (15).…”

mentioning

confidence: 99%

Streptococcus sanguisModulates Type II Collagen-Induced Arthritis in DBA/1J Mice

Costalonga

Hodges

Herzberg

2002

The Journal of Immunology

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Native type II collagen is tolerogenic when given orally or i.p. to DBA/1J mice and induces autoimmune arthritis when given s.c. in CFA. The tolerogenic epitope is contained in cyanogen bromide fragment 11 (CB11) and is structurally mimicked by PGEQGPK within the platelet aggregation-associated protein (PAAP) on Streptococcus sanguis. To learn whether S. sanguis modulates transmucosally the Ag-specific development of autoimmune arthritis, DBA/1J pups were given live S. sanguis, CB11, or type II collagen intragastrically. Feeding S. sanguis at 6 days postpartum delayed the onset of arthritis, and reduced the rate, final severity, and percentage of affected limbs. Next, PAAP+ S. sanguis and type II collagen were tested for T cell cross-reactivity. T cells primed with the tolerogenic epitope of type II collagen proliferated more when incubated with PAAP+ S. sanguis than with PAAP− Streptococcus gordonii or type II collagen, suggesting an Ag-specific transmucosal tolerogenic effect. In neonatal mice, therefore, bacterial surface Ags that mimic self can transmucosally stimulate Ag-specific inhibitory T cells. In adult mice immunized with type II collagen, these Ag-specific inhibitory T cells manifest later as attenuated arthritis. The PAAP+ S. sanguis appear to activate adult memory, rather than naive, type II collagen-specific T cells, suggesting that systemic challenge with commensal self-mimicking microorganisms may perpetuate existing autoimmunity, but not initiate autorecognition.

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Dental Flossing and Its Relationship to Transient Bacteremia

Cited by 90 publications

References 10 publications

Porphyromonas gingivalis Infection Accelerates the Progression of Atherosclerosis in a Heterozygous Apolipoprotein E–Deficient Murine Model

Porphyromonas gingivalis Infection Accelerates the Progression of Atherosclerosis in a Heterozygous Apolipoprotein E–Deficient Murine Model

Autophagy: A Highway for Porphyromonas gingivalis in Endothelial Cells

Streptococcus sanguisModulates Type II Collagen-Induced Arthritis in DBA/1J Mice

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